Pain is a designation for a spectrum of sensations of highly divergent character and intensity ranging from unpleasant to intolerable. Pain stimuli are detected by physiological receptors (sensors, nociceptors) least differentiated morphologically, viz., free nerve endings. The body of the bipolar afferent first-order neuron lies in a dorsal root ganglion. Nociceptive impulses are conducted via unmyelinated (C-fibers, conduction velocity 0.2-2.0 m/s) and myelinated axons (A8-fibers, 5-30 m/s). The free endings of AS fibers respond to intense pressure or heat, those of C-fibers respond to chemical stimuli (H+, K+, histamine, bradykinin, etc.) arising from tissue trauma. Irrespective of whether chemical, mechanical, or thermal stimuli are involved, they become significantly more effective in the presence of prostaglandins (p. 196).
Chemical stimuli also underlie pain secondary to inflammation or ischemia (angina pectoris, myocardial infarction), or the intense pain that occurs during overdistention or spasmodic contraction of smooth muscle abdominal organs, and that may be maintained by local anoxemia developing in the area of spasm (visceral pain).
AS and C-fibers enter the spinal cord via the dorsal root, ascend in the dorsolateral funiculus, and then synapse on second-order neurons in the dorsal horn. The axons of the second-order neurons cross the midline and ascend to the brain as the anterolateral pathway or spinothalamic tract. Based on phylogenetic age, neo- and paleospi-nothalamic tracts are distinguished. Thalamic nuclei receiving neospinotha-lamic input project to circumscribed areas of the postcentral gyrus. Stimuli conveyed via this path are experienced as sharp, clearly localizable pain. The nuclear regions receiving paleospino-thalamic input project to the postcentral gyrus as well as the frontal, limbic cortex and most likely represent the pathway subserving pain of a dull, ach ing, or burning character, i.e., pain that can be localized only poorly.
Impulse traffic in the neo- and pa-leospinothalamic pathways is subject to modulation by descending projections that originate from the reticular formation and terminate at second-order neurons, at their synapses with first-order neurons, or at spinal segmental inter-neurons (descending antinociceptive system). This system can inhibit impulse transmission from first- to second-order neurons via release of opio-peptides (enkephalins) or monoamines (norepinephrine, serotonin).
Pain sensation can be influenced or modified as follows:
• elimination of the cause of pain
• lowering of the sensitivity of noci-ceptors (antipyretic analgesics, local anesthetics)
• interrupting nociceptive conduction in sensory nerves (local anesthetics)
• suppression of transmission of noci-ceptive impulses in the spinal medulla (opioids)
• inhibition of pain perception (opi-oids, general anesthetics)
• altering emotional responses to pain, i.e., pain behavior (antidepress-ants as "co-analgesics," p. 230).
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